This project encompasses studies aimed at analyzing the participation of macrophages and their products in processes which affect the eye or other tissues. The experiments reported here were a continuation of the ongoing study concerning interleukin 1 (IL-1), a macrophage product which plays a major role in mediating certain immune responses, inflammatory processes, and wound healing. Noteworthy findings: (1) Previous studies have shown that macrophages may retain high levels of intracellular IL-1 and that this pool of IL-1 differs by certain aspects from the extracellular pool, which is released into the medium. The present experiments have revealed that the two pools of IL-1 also differ markedly in their molecular charge, as demonstrated by their isoelectrofocusing profile. A major portion (about 60%) of the extracellular pool has an isoelectric point (pI) of 6.7, while smaller portions are characterized by pIs of 5.5 and 6.1. On the other hand, about 90% of the intracellular IL-1 pool was found to have a pI of 5.5 and only minor portions were found with pI of 6.7 or 6.1. (2) We have previously proposed that intracellular IL-1 is mainly involved in facilitating the immune response while the xtracellular pool's function is to mediate the body's reaction to injury or inflammation. This hypothesis was examined by measureing the levels of extracellular and intracellular IL-1 activities in macrophage cultures stimulated with lipopolysaccharide (endotoxin) or one of its components, lipid A, which was treated to lose its capacity to cause fever but to retain its immune enhancing capacity. The detoxified lipid A was found to selectively increase the intracellular IL-1 activity while having less effect on the extracellular pool. On the other hand, untreated lipid A, or the whole lipopolysaccharide molecule, stimulated similar levels of both intracellular and extracellular IL-1 activities. The data are interpreted to support the aforementioned hypothesis by showing a correlation between the capacity to increase the intracellular IL-1 and immune enhancement.